INTRODUCTION

In the human kidney, some 1 million glomeruli filter 180 liters of plasma daily, allowing passage of low-molecular-weight products while restricting the passage of albumin and larger macromolecules. The resulting urine is extensively modified in the renal tubular system, with changes to both composition and volume necessary to maintain extracellular volume and homeostasis. As a consequence of this, immune complexes formed in the circulation are delivered at a high rate to the intraglomerular capillary bed and trapping occurs primarily in the mesangium and or on the subendothelial surface of the capillary wall. In contrast to in vitro models, which are somewhat limited to assessing isolated cell, antibody, and antigen function, or indeed, human biopsy specimens which give a snapshot at a particular clinical stage, in vivo animal models can outline how structure and function changes with initiation, progression, and potential regression within affected organs and the various cellular and humoral factors involved in disease progression. The nephron is the functioning unit of the kidney and the glomerulus is a branching network of capillaries responsible for plasma filtration and the initial step in urine formation. This chapter will review the use of experimental animal models in delineating the pathogenesis of glomerulonephritis (GN). GN at its basic definition is the term used to describe an inflammatory process involving the glomeruli characterized morphologically by an influx of leucocytes and cellular proliferation often accompanied by glomerular capillary wall abnormalities.